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Cholecystitis
Lecture 31
• Cholecystitis (Greek, -cholecyst, "gallbladder",
combined with the suffix -itis, "inflammation")
is inflammation of the gallbladder, which
occurs most commonly due to obstruction of
the cystic duct with gallstones (cholelithiasis).
Classification
• Acute: calculous & acalculous
• Chronic
• Acute superimposed on chronic
Acute Cholecystitis
• Acute calculous cholecystitis is an acute
inflammation of the gallbladder, precipitated
90% of the time by obstruction of the neck or
cystic duct.
• It is the primary complication of gallstones
and the most common reason for emergency
cholecystectomy.
Aacalculous cholecystitis
• Cholecystitis without gallstones called
acalculous cholecystitis may occur in severely
ill patients and accounts for about 10% of
patients with cholecystitis.
Pathogenesis.
• Acute calculous cholecystitis results from
chemical irritation and inflammation of the
obstructed gallbladder.
• The action of mucosal phospholipases
hydrolyzes luminal lecithins to toxic
lysolecithins.
• The normally protective glycoprotein mucus
layer is disrupted, exposing the mucosal
epithelium to the direct detergent action of
bile salts.
• Prostaglandins released within the wall of the
distended gallbladder contribute to mucosal and
mural inflammation.
• Gallbladder dysmotility develops; distention
and increased intraluminal pressure
compromise blood flow to the mucosa.
• Acute calculous cholecystitis frequently
develops in diabeticpatients who
have symptomatic gallstones.
Pathogenesis
• Acute acalculous cholecystitis is thought to result
from ischemia. The cystic artery is an end artery
with essentially no collateral circulation.
Risk factors for acute acalculous
cholecystitis include:
(1) Sepsis with hypotension and multisystem
organ failure;
(2) Immunosuppression;
(3) Major trauma and burns;
(4) Diabetes mellitus; and
(5) Infections.
Morphology.
In acute cholecystitis the gallbladder is usually
enlarged and tense, and it may assume a
bright red or blotchy, violaceous to green-
black discoloration, imparted by subserosal
hemorrhages.
• The serosal covering is frequently layered by
fibrin and, in severe cases, by a definite
suppurative, coagulated exudate.
Morphology
• In calculous cholecystitis, an obstructing
stone is usually present in the neck of the
gallbladder or the cystic duct.
• The gallbladder lumen may contain one or
more stones and is filled with a cloudy or
turbid bile that may contain large amounts of
fibrin, pus, and hemorrhage.
• In mild cases the gallbladder wallis
thickened, edematous, and hyperemic.
• In more severe cases it is transformed into a
green-black necrotic organ, termed
gangrenous cholecystitis,
with small-to-large perforations.
• The invasion of gas-forming organisms,
notably clostridia and coliforms, may cause
an acute “emphysematous” cholecystitis.
Clinical Features.
• An attack of acute cholecystitis begins with
progressive right upper quadrant or
epigastric pain, frequently associated with
mild fever, anorexia, tachycardia, sweating,
nausea, and vomiting.
• The pain may be referred pain that is felt in
the right scapula rather than the right upper
quadrant or epigastric region (Boas' sign).
• It may also correlate with eating greasy, fatty,
or fried foods.
• The Murphy sign is specific, but not sensitive
for cholecystitis.
• Elderly patients and those with diabetes may
have vague symptoms that may not include
fever or localized tenderness.
• More severe symptoms such as high fever,
shock and jaundice indicate the development
of complications such as
• abscess formation,
• perforation or
• ascending cholangitis.
• Another complication, gallstone ileus,
occurs if the gallbladder perforates and forms
a fistula with the nearby small bowel, leading
to symptoms of intestinal obstruction.
• Clinical symptoms of acute acalculous
cholecystitis tend to be more insidious, since
symptoms are obscured by the underlying
conditions precipitating the attacks.
• As a result of either delay in diagnosis or the
disease itself, the incidence of gangrene and
perforation is much higher in acalculous than
in calculous cholecystitis.
Chronic Cholecystitis
• Chronic cholecystitis may be a sequel to
repeated bouts of mild to severe acute
cholecystitis,
• but in many instances it develops in the
apparent absence of antecedent attacks.
• Since it is associated with cholelithiasis in
more than 90% of cases, the patient
populations are the same as those for
gallstones.
• supersaturation of bile
predisposes to both chronic inflammation
and, in most instances, stone formation.
• Unlike acute calculous cholecystitis,
obstruction of gallbladder outflow is not a
requisite.
• , the symptoms of calculous chronic
cholecystitis are biliary colic to indolent right
upper quadrant pain and epigastric distress.
Morphology.
• The morphologic changes in chronic
cholecystitis are extremely variable and
sometimes minimal.
• The serosa is usually smooth and
glistening but may be dulled by subserosal
fibrosis.
• Dense fibrous adhesions
• On sectioning, the wall is variably thickened,
and has an opaque gray-white appearance.
• In the uncomplicated case
• the lumen contains fairly clear, green-yellow,
mucoid bile and usually stones. The mucosa
itself is generally preserved.
Microscopy
• In the mildest cases, only scattered
lymphocytes, plasma cells, and macrophages
are found in the mucosa and in the
subserosal fibrous tissue.
• In more advanced cases there is
marked subepithelial and subserosal
fibrosis, accompanied by mononuclear
cell infiltration.
• Outpouchings of the mucosal epithelium
through the wall
(Rokitansky-Aschoff
sinuses) may be quite prominent.
Acute superimposed on chronic
cholecystitis
Superimposition of acute
inflammatory changes implies
acute exacerbation of an already chronically
injured gallbladder.
Porcelain gallbladder
• In rare instances extensive dystrophic
calcificatio
n within the gallbladder wall may yield a
porcelain gallbladder, notable for a markedly
increased incidence of associated cancer.
• Xanthogranulomatous cholecystitis is also a
rare condition in which the gallbladder has a
massively thickened wall, is
shrunken, nodular, and chronically inflamed
with foci of necrosis and hemorrhage.
• Finally, an atrophic, chronically
obstructed gallbladder may
contain only clear secretions, a
condition known as
hydrops of the gallbladder.
Clinical Features.
• Usually characterized by recurrent attacks of
either steady or colicky epigastric or right
upper quadrant pain.
• Nausea, vomiting, and intolerance for fatty
foods are frequent accompaniments.
L31 cholecystitis students

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L31 cholecystitis students

  • 2. • Cholecystitis (Greek, -cholecyst, "gallbladder", combined with the suffix -itis, "inflammation") is inflammation of the gallbladder, which occurs most commonly due to obstruction of the cystic duct with gallstones (cholelithiasis).
  • 3. Classification • Acute: calculous & acalculous • Chronic • Acute superimposed on chronic
  • 4.
  • 5. Acute Cholecystitis • Acute calculous cholecystitis is an acute inflammation of the gallbladder, precipitated 90% of the time by obstruction of the neck or cystic duct. • It is the primary complication of gallstones and the most common reason for emergency cholecystectomy.
  • 6. Aacalculous cholecystitis • Cholecystitis without gallstones called acalculous cholecystitis may occur in severely ill patients and accounts for about 10% of patients with cholecystitis.
  • 7. Pathogenesis. • Acute calculous cholecystitis results from chemical irritation and inflammation of the obstructed gallbladder.
  • 8. • The action of mucosal phospholipases hydrolyzes luminal lecithins to toxic lysolecithins.
  • 9. • The normally protective glycoprotein mucus layer is disrupted, exposing the mucosal epithelium to the direct detergent action of bile salts.
  • 10. • Prostaglandins released within the wall of the distended gallbladder contribute to mucosal and mural inflammation.
  • 11. • Gallbladder dysmotility develops; distention and increased intraluminal pressure compromise blood flow to the mucosa.
  • 12. • Acute calculous cholecystitis frequently develops in diabeticpatients who have symptomatic gallstones.
  • 13.
  • 14. Pathogenesis • Acute acalculous cholecystitis is thought to result from ischemia. The cystic artery is an end artery with essentially no collateral circulation.
  • 15. Risk factors for acute acalculous cholecystitis include: (1) Sepsis with hypotension and multisystem organ failure; (2) Immunosuppression; (3) Major trauma and burns; (4) Diabetes mellitus; and (5) Infections.
  • 16. Morphology. In acute cholecystitis the gallbladder is usually enlarged and tense, and it may assume a bright red or blotchy, violaceous to green- black discoloration, imparted by subserosal hemorrhages.
  • 17. • The serosal covering is frequently layered by fibrin and, in severe cases, by a definite suppurative, coagulated exudate.
  • 18.
  • 19.
  • 20.
  • 21. Morphology • In calculous cholecystitis, an obstructing stone is usually present in the neck of the gallbladder or the cystic duct.
  • 22. • The gallbladder lumen may contain one or more stones and is filled with a cloudy or turbid bile that may contain large amounts of fibrin, pus, and hemorrhage.
  • 23. • In mild cases the gallbladder wallis thickened, edematous, and hyperemic.
  • 24. • In more severe cases it is transformed into a green-black necrotic organ, termed gangrenous cholecystitis, with small-to-large perforations.
  • 25. • The invasion of gas-forming organisms, notably clostridia and coliforms, may cause an acute “emphysematous” cholecystitis.
  • 26. Clinical Features. • An attack of acute cholecystitis begins with progressive right upper quadrant or epigastric pain, frequently associated with mild fever, anorexia, tachycardia, sweating, nausea, and vomiting.
  • 27.
  • 28. • The pain may be referred pain that is felt in the right scapula rather than the right upper quadrant or epigastric region (Boas' sign).
  • 29. • It may also correlate with eating greasy, fatty, or fried foods.
  • 30. • The Murphy sign is specific, but not sensitive for cholecystitis.
  • 31. • Elderly patients and those with diabetes may have vague symptoms that may not include fever or localized tenderness.
  • 32. • More severe symptoms such as high fever, shock and jaundice indicate the development of complications such as • abscess formation, • perforation or • ascending cholangitis.
  • 33. • Another complication, gallstone ileus, occurs if the gallbladder perforates and forms a fistula with the nearby small bowel, leading to symptoms of intestinal obstruction.
  • 34. • Clinical symptoms of acute acalculous cholecystitis tend to be more insidious, since symptoms are obscured by the underlying conditions precipitating the attacks.
  • 35. • As a result of either delay in diagnosis or the disease itself, the incidence of gangrene and perforation is much higher in acalculous than in calculous cholecystitis.
  • 36.
  • 37. Chronic Cholecystitis • Chronic cholecystitis may be a sequel to repeated bouts of mild to severe acute cholecystitis, • but in many instances it develops in the apparent absence of antecedent attacks.
  • 38. • Since it is associated with cholelithiasis in more than 90% of cases, the patient populations are the same as those for gallstones.
  • 39. • supersaturation of bile predisposes to both chronic inflammation and, in most instances, stone formation.
  • 40. • Unlike acute calculous cholecystitis, obstruction of gallbladder outflow is not a requisite.
  • 41. • , the symptoms of calculous chronic cholecystitis are biliary colic to indolent right upper quadrant pain and epigastric distress.
  • 42. Morphology. • The morphologic changes in chronic cholecystitis are extremely variable and sometimes minimal.
  • 43. • The serosa is usually smooth and glistening but may be dulled by subserosal fibrosis. • Dense fibrous adhesions
  • 44. • On sectioning, the wall is variably thickened, and has an opaque gray-white appearance.
  • 45. • In the uncomplicated case • the lumen contains fairly clear, green-yellow, mucoid bile and usually stones. The mucosa itself is generally preserved.
  • 46. Microscopy • In the mildest cases, only scattered lymphocytes, plasma cells, and macrophages are found in the mucosa and in the subserosal fibrous tissue.
  • 47. • In more advanced cases there is marked subepithelial and subserosal fibrosis, accompanied by mononuclear cell infiltration.
  • 48. • Outpouchings of the mucosal epithelium through the wall (Rokitansky-Aschoff sinuses) may be quite prominent.
  • 49.
  • 50. Acute superimposed on chronic cholecystitis Superimposition of acute inflammatory changes implies acute exacerbation of an already chronically injured gallbladder.
  • 51. Porcelain gallbladder • In rare instances extensive dystrophic calcificatio n within the gallbladder wall may yield a porcelain gallbladder, notable for a markedly increased incidence of associated cancer.
  • 52.
  • 53. • Xanthogranulomatous cholecystitis is also a rare condition in which the gallbladder has a massively thickened wall, is shrunken, nodular, and chronically inflamed with foci of necrosis and hemorrhage.
  • 54. • Finally, an atrophic, chronically obstructed gallbladder may contain only clear secretions, a condition known as hydrops of the gallbladder.
  • 55. Clinical Features. • Usually characterized by recurrent attacks of either steady or colicky epigastric or right upper quadrant pain.
  • 56. • Nausea, vomiting, and intolerance for fatty foods are frequent accompaniments.